Posts Tagged ‘Alzheimer’s disease’

New evidence suggests a mechanism by which progressive accumulation of Tau protein in brain cells may lead to Alzheimer’s disease. Scientists studied more than 600 human brains and fruit fly models of Alzheimer’s disease and found the first evidence of a strong link between Tau protein within neurons and the activity of particular DNA sequences called transposable elements, which might trigger neurodegeneration. The study appears in the journal Cell Reports.

“One of the key characteristics of Alzheimer’s disease is the accumulation of Tau protein within brain cells, in combination with progressive cell death,” said corresponding author Dr. Joshua Shulman, associate professor of neurology, neuroscience and molecular and human genetics at Baylor College of Medicine and investigator at the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital. “In this study we provide novel insights into how accumulation of Tau protein may contribute to the development of Alzheimer’s disease.”

Although scientists have studied for years what happens when Tau forms aggregates inside neurons, it still is not clear why brain cells ultimately die. One thing that scientists have noticed is that neurons affected by Tau accumulation also appear to have genomic instability.

“Genomic instability refers to an increased tendency to have alterations in the genetic material, DNA, such as mutations or other impairments. This means that the genome is not functioning correctly. Genomic instability is known to be a major driving force behind other diseases such as cancer,” Shulman said. “Our study focused on a new possible causal connection between Tau accumulation within neurons and the resulting genomic instability in Alzheimer’s disease.”

Enter transposable elements
Previous studies of brain tissues from patients with other neurologic diseases and of animal models have suggested that the neurons not only present with genomic instability, but also with activation of transposable elements.

“Transposable elements are short pieces of DNA that do not seem to contribute to the production of proteins that make cells function. They behave in a way similar to viruses; they can make copies of themselves that are inserted within the genome and this can create mutations that lead to disease,” Shulman said. “Although most transposable elements are dormant or dysfunctional, some may become active in human brains late in life or in disease. That’s what led us to look specifically at Alzheimer’s disease and the possible association between Tau accumulation and activated transposable elements.”

Shulman and his colleagues began their investigations by studying more than 600 human brains from a population study run by co-author Dr. David Bennett at Rush University Medical Center in Chicago. This population study follows participants throughout their lives and at death, allowing the researchers to examine their brains in detail postmortem. One of the evaluations is the amount of Tau accumulation across many brain regions. In addition, co-author Dr. Philip De Jager at the Broad Institute and Columbia University comprehensively profiled gene expression in the same brains.

“With this large amount of data, we looked to identify signatures of active transposable elements, but this was not easy,” Shulman said. “We therefore reached out to Dr. Zhandong Liu, a co-author in this study, and together we developed a new software tool to detect signatures of active transposable elements from postmortem human brains. Then we conducted a statistical analysis in which we compared the amount of active transposable elements signatures with the amount of Tau accumulation, brain by brain.” Liu also is assistant professor of pediatrics – neurology at Baylor and a member of the Dan L Duncan Comprehensive Cancer Center.

The researchers found a strong link between the amount of Tau accumulation in neurons and detectable activity of transposable elements.

“We identified individual transposable elements that were active when Tau aggregates were present. Surprisingly, we also found evidence that the activation of transposable elements was quite broad across the genome,” Shulman said.

Other research has shown that Tau may disrupt the tightly packed architecture of the genome. It is believed that tightly packed DNA limits gene activation, while opening up the DNA may promote it. Keeping the DNA tightly packed may be an important mechanism to suppress the activity of transposable elements that lead to disease.

“The fact that Tau aggregates can affect that architecture of the genome may be one possible mechanism by which transposable elements are activated in Alzheimer’s disease,” Shulman said. “However, our studies in human brains only establish an association between Tau accumulation and activation of transposable elements. To determine whether Tau accumulation could in fact cause transposable element activation, we conducted studies with a fruit fly model of Alzheimer’s disease.”

In this fruit fly model of the disease, the researchers found that triggering Tau changes similar to those observed in human brains resulted in the activation of fruit fly transposable elements, strongly suggesting that Tau aggregates that disrupt the architecture of the genome can potentially mediate the activation of transposable elements and ultimately cause neurodegeneration.

“We think our experiments reveal new and potentially important insights relevant for understanding Alzheimer’s disease mechanisms,” Shulman said. “There is still a lot of work to be done, but by presenting our results we hope we can stimulate others in the research community to help work on this problem.”

https://www.bcm.edu/news/neurology/research-links-tau-aggregates-cell-death

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Brown University researchers studying the biology of aging have demonstrated a new strategy for stimulating autophagy, the process by which cells rebuild themselves by recycling their own worn-out parts.

In a study published in the journal Cell Reports, the researchers show that the approach increased the lifespans of worms and flies, and experiments in human cells hint that the strategy could be useful in future treatments for Alzheimer’s disease, ALS and other age-related neurodegenerative conditions.

“Autophagy dysfunction is present across a range of age-related diseases including neurodegeneration,” said Louis Lapierre, an assistant professor of molecular biology, cell biology and biochemistry at Brown who led the work. “We and others think that by learning how to influence this process pharmacologically, we might be able to affect the progression of these diseases. What we’ve shown here is a new and conserved entry point for stimulating autophagy.”

Autophagy has become a hot topic in recent years, earning its discoverer the Nobel Prize in Physiology and Medicine in 2016. The process involves the rounding up of misfolded proteins and obsolete organelles within a cell into vesicles called autophagosomes. The autophagosomes then fuse with a lysosome, an enzyme-containing organelle that breaks down those cellular macromolecules and converts it into components the cell can re-use.

Lapierre and his colleagues wanted to see if they could increase autophagy by manipulating a transcription factor (a protein that turns gene expression on and off) that regulates autophagic activity. In order for the transcription factor to switch autophagic activity on, it needs to be localized in the nucleus of a cell. So Lapierre and his team screened for genes that enhance the level of the autophagy transcription factor, known as TFEB, within nuclei.

Using the nematode C. elegans, the screen found that reducing the expression of a protein called XPO1, which transports proteins out of the nucleus, leads to nuclear accumulation of the nematode version of TFEB. That accumulation was associated with an increase in markers of autophagy, including increased autophagosome, autolysosomes as well as increased lysosome biogenesis. There was also a marked increase in lifespan among the treated nematodes of between about 15 and 45 percent.

“What we showed was that by blocking the escape of this transcription factor from the nucleus, we could not only influence autophagy but we could get an increase in lifespan as well,” Lapierre said.

The next step was to see if there were drugs that could mimic the effect of the gene inhibition used in the screening experiment. The researchers found that selective inhibitors of nuclear export (SINE), originally developed to inhibit XPO1 to treat cancers, had a similar effect — increasing markers of autophagy and significantly increasing lifespan in nematodes.

The researchers then tested SINE on a genetically modified fruit fly that serves as a model organism for the neurodegenerative disease ALS. Those experiments showed a small but significant increase in the lifespans of the treated flies. “Our data suggests that these compounds can alleviate some of the neurodegeneration in these flies,” Lapierre said.

As a final step, the researchers set out to see if XPO1 inhibition had similar effects on autophagy in human cells as it had in the nematodes. After treating a culture of human HeLa cells with SINE, the researchers found that, indeed, TFEB concentrations in nuclei increased, as did markers of autophagic activity and lysosomal biogenesis.

“Our study tells us that the regulation of the intracellular partitioning of TFEB is conserved from nematodes to humans and that SINE could stimulate autophagy in humans,” Lapierre said. “SINE have been recently shown in clinical trials for cancer to be tolerated, so the potential for using SINE to treat other age-related diseases is there.”

Future research, Lapierre said, will focus on testing these drugs in more clinically relevant models of neurodegenerative diseases. But this initial research is a proof of concept for this strategy as a means to increase autophagy and potentially treat age-related diseases.

Lapierre is a faculty member in the newly approved Center on the Biology of Aging within the Brown Institute for Translational Science. This center, led by Professor of Biology John Sedivy, studies the biological mechanisms of aging. The center’s mission is to expand biomedical research and education programs in the emerging discipline of biogerontology, and to bring forth scientific discoveries related to aging and associated disorders.

Neuroscientists at Indiana University have reported the first evidence that non-human animals can mentally replay past events from memory. The discovery could help advance the development of new drugs to treat Alzheimer’s disease.

The study, led by IU professor Jonathon Crystal, appears today in the journal Current Biology.

“The reason we’re interested in animal memory isn’t only to understand animals, but rather to develop new models of memory that match up with the types of memory impaired in human diseases such as Alzheimer’s disease,” said Crystal, a professor in the IU Bloomington College of Arts and Sciences’ Department of Psychological and Brain Sciences and director of the IU Bloomington Program in Neuroscience.

Under the current paradigm, Crystal said most preclinical studies on potential new Alzheimer’s drugs examine how these compounds affect spatial memory, one of the easiest types of memory to assess in animals. But spatial memory is not the type of memory whose loss causes the most debilitating effects of Alzheimer’s disease.

“If your grandmother is suffering from Alzheimer’s, one of the most heartbreaking aspects of the disease is that she can’t remember what you told her about what’s happening in your life the last time you saw her,” said Danielle Panoz-Brown, an IU Ph.D. student who is the first author on the study. “We’re interested in episodic memory — and episodic memory replay — because it declines in Alzheimer’s disease, and in aging in general.”

Episodic memory is the ability to remember specific events. For example, if a person loses their car keys, they might try to recall every single step — or “episode” — in their trip from the car to their current location. The ability to replay these events in order is known as “episodic memory replay.” People wouldn’t be able to make sense of most scenarios if they couldn’t remember the order in which they occurred, Crystal said.

To assess animals’ ability to replay past events from memory, Crystal’s lab spent nearly a year working with 13 rats, which they trained to memorize a list of up to 12 different odors. The rats were placed inside an “arena” with different odors and rewarded when they identified the second-to-last odor or fourth-to-last odor in the list.

The team changed the number of odors in the list before each test to confirm the odors were identified based upon their position in the list, not by scent alone, proving the animals were relying on their ability to recall the whole list in order. Arenas with different patterns were used to communicate to the rats which of the two options was sought.

After their training, Crystal said, the animals successfully completed their task about 87 percent of the time across all trials. The results are strong evidence the animals were employing episodic memory replay.

Additional experiments confirmed the rats’ memories were long-lasting and resistant to “interference” from other memories, both hallmarks of episodic memory. They also ran tests that temporarily suppressed activity in the hippocampus — the site of episodic memory — to confirm the rats were using this part of their brain to perform their tasks.

Crystal said the need to find reliable ways to test episodic memory replay in rats is urgent since new genetic tools are enabling scientists to create rats with neurological conditions similar to Alzheimer’s disease. Until recently, only mice were available with the genetic modifications needed to study the effect of new drugs on these symptoms.

“We’re really trying push the boundaries of animal models of memory to something that’s increasingly similar to how these memories work in people,” he said. “If we want to eliminate Alzheimer’s disease, we really need to make sure we’re trying to protect the right type of memory.”

https://news.iu.edu/stories/2018/05/iub/releases/10-scientists-find-first-evidence-animals-can-mentally-replay-past-events.html

On the heels of one failed drug trial after another, a recent study suggests people with early Alzheimer’s disease could reap modest benefits from a device that uses magnetic fields to produce small electric currents in the brain.

Alzheimer’s is a degenerative brain disorder that afflicts more than 46 million people worldwide. At present there are no treatments that stop or slow its progression, although several approved drugs offer temporary relief from memory loss and other cognitive symptoms by preventing the breakdown of chemical messengers among nerve cells.

The new study tested a regimen that combines computerized cognitive training with a procedure known as repetitive transcranial magnetic stimulation (rTMS). The U.S. Food and Drug Administration has cleared rTMS devices for some migraine sufferers as well as for people with depression who have not responded to antidepressant medications.

Israel-based Neuronix reported results of a phase III clinical trial of its therapy system, known as neuroAD, in Alzheimer’s patients. More than 99 percent of Alzheimer’s drug trials have failed. The last time a phase III trial for a wholly new treatment succeeded (not just a combination of two already approved drugs) was about 15 years ago. The recent study did not test a drug but rather a device, which usually has an easier time gaining FDA clearance. NeuroAD has been approved for use in Europe and the U.K., where six weeks of therapy costs about $6,700. The system is not commercially available in the U.S., but based on the latest results the company submitted an application for FDA clearance last fall.

The neuroAD setup resembles a dental chair fitted with a touch screen and flexible arms, which generate magnetic fields from metal coils positioned near the person’s scalp. The magnetic fields produce electric currents within the brain that influence the activity of neurons. The procedure can reportedly speed up learning by strengthening synaptic connections between neurons while the person performs tasks that engage those particular brain cells. In the cognitive training that accompanies rTMS, when study participants see a picture of a strawberry and touch the screen to identify it as “fruit” or “furniture,” for instance, the system stimulates Wernicke’s area, the brain region responsible for language comprehension.

For its latest rTMS trial, the company enrolled about 130 people with mild to moderate Alzheimer’s at 10 sites—nine in the U.S. and one in Israel. Four out of five participants were already taking symptom-relieving therapies. At the start of the trial, each person took a cognitive battery—a 30-minute paper-and-pencil test commonly used to gauge mental function in Alzheimer’s studies—and was randomly assigned to receive the rTMS-cognitive therapy or a sham treatment for six weeks. The sessions lasted about an hour each day, five days per week.

A week after the six-week regimen, and again five weeks later, participants retook the paper-and-pencil test to see if their cognition improved. Despite the elaborate protocol, study adherence was high. More than 90 percent of participants completed at least 90 percent of their visits, says Babak Tousi, who heads the Clinical Trials Program at Cleveland Clinic Lou Ruvo Center for Brain Health and reported the trial’s results at the Vienna meeting.

Based on past studies of the neuroAD system in smaller groups (none had more than 30 participants), the company expected to see a cognitive benefit after six weeks of treatment. Curiously, though, the recent study revealed no significant difference in test scores between active and sham groups at the seven-week time point. (The sham group sat in the chair and saw pictures on the screen but received no cognitive training or exposure to magnetic fields.) At week 12—six weeks after the therapy ended—the active group did show an 1.8-point test score advantage over the sham group. “That is a pretty small effect,” says Lon Schneider, who directs the State of California Alzheimer’s Disease Center at the University of Southern California in Los Angeles and heard the study results presented in Vienna. By comparison, he says, drugs currently approved to treat Alzheimer’s symptoms have shown a 2.5- to 3-point improvement in six-month clinical trials. And in a study reported last fall, a leading pharmaceutical candidate tested in more than 2,100 people seemed to work about as well (a roughly 1.5-point improvement) but failed to achieve statistical significance.

Plus, the modest effect seen with the new rTMS trial only turned up in participants with mild Alzheimer’s, Tousi reported. People with more advanced cases did not improve on the therapy. “We’ve got that typical problem of a small study that does seem to give outcomes, but the outcomes are either unclear or not fully evaluable,” Schneider says, adding it is unclear, for instance, if the test scores improved because of the cognitive training or resulted from possible mood-enhancing effects of the rTMS, because some Alzheimer’s patients have depression or other psychiatric symptoms.

John-Paul Taylor, a neuropsychiatrist at Newcastle University in England who was not involved with the study and researches TMS’s prospects for treating visual hallucinations in dementia, agrees that it is hard to tell if the cognitive improvement was indeed “a real TMS effect.” He says, however, this technology is “ripe for more investigation.”

Taylor is working with colleagues who are trying to use computational modeling to get a better idea how rTMS works. “That’s where it’s going to get really interesting,” he says. “I suspect you’ll have to tailor the stimulation to individual patients.” Consistent with that idea, earlier this year researchers reported using brain imaging to identify different types of depression—and patients in one of those subgroups responded especially well to rTMS.

With the computational modeling, one could imagine feeding in a person’s brain scan “and the computer would say, you need to be in this position at this stimulation intensity to equal what another person would receive,” Taylor says. “That’s not that far off.” Ultimately, though, “we want a therapeutic that still works across everybody to some degree,” he says. “There’s a hint of that in this trial. I’m cautiously optimistic.”

https://www.scientificamerican.com/article/could-magnetic-brain-stimulation-help-people-with-alzheimer-rsquo-s/

A research team at University of Copenhagen including a researcher from the Faculty of Health and Medical Sciences has discovered a circuit in the brains of mice connecting circadian rhythm to aggressive behaviour. The discovery is particularly interesting to Alzheimer’s patients who experience increased aggression at night. The researchers have developed special protein tools capable of turning off the cells in the brain causing the behaviour.

Each year around 8,000 Danes are diagnosed with a form of dementia. Alzheimer’s disease is one of them. The disease manifests itself in memory difficulties in particular, but can also result in personality changes and mood swings.

When the sun sets 20 per cent of all Alzheimer’s patients experience increased bewilderment, anxiety, unease, disorientation, irritation and aggression. This phenomenon is called ‘sundowning’ or sundown syndrome. At worst, the condition can mean that the patient must be left in professional care, as it can be difficult for family members to handle. The cause of the condition is unknown, but previous research has suggested that it is connected to the circadian rhythm.

A research team including a researcher from the Department of Drug Design and Pharmacology at the University of Copenhagen is now able to confirm this connection. The researchers have identified and mapped a circuit between the part of the brain containing the circadian clock or circadian rhythm and a part of the brain controlling aggression.

’We have shown that the circadian clock in mice is closely linked to an aggression centre in the mouse brain by a cell circuit. The human brain has those same groups of cells that the circuit goes through. With this knowledge, we are now enabled to target this circuit pharmacologically and target cells that make people aggressive at the end of the day’, says Assistant Professor Timothy Lynagh from the Department of Drug Design and Pharmacology at the University of Copenhagen.

Turn off the Aggression
The inner clock or circadian rhythm is located in the part of the brain called suprachiasmatic nucleus. One of the parts of the brain that control aggressive behaviour is called the ventromedial hypothalamus. Researchers have previously observed a connection between the two parts of the brain, though none have had knowledge of the specific circuit connecting them.

Using electrophysiology and microscopy, the researchers measured the activity of the brain cells at main author Clifford Saper’s laboratory in Boston. They also turned off parts of the cell circuit in the brains of mice to map the circuit and to identify the cells connecting the two parts of the brain. To map circuits in the brain you need a protein tool that can turn off the various cells to determine their function. Assistant Professor Timothy Lynagh has designed precisely such a tool.

‘We take a receptor and mutate it, so that it is not sensitive to anything in the brain, but very sensitive to a particular drug. The tool works like an on/off switch. When you put the protein tool in the mouse brain, under normal circumstances, nothing will happen. But when you give the animal the drug, the cells that have the receptor on them will be turned off’, Timothy Lynagh explains.

Using this tool, the researchers can thus in theory turn off the cells that cause people suffering from sundown syndrome to become more aggressive at night.

May Be Used on Humans 20 Years into the Future
The tool can also be used in other contexts than sundown syndrome. In other studies, Tim Lynagh’s tool has been used to turn off cells in rats linked to anxiety and fear.

‘If you can start understanding which cells in the brain lead to which problems, you can then put this tool into any of those parts of the brain. The person who takes the drug will then have the cells causing the problem turned off’, Timothy Lynagh says.

Even though the study was conducted on mice, the tool and the knowledge the research has generated can potentially be used in the treatment of humans.

‘Because of the huge advances that are coming along with CRISPR, I would be tempted to say that based on a recent demonstration of gene therapy for brain disease, potentially, it could be used in the human brain in 20 years’ time. Of course it needs a lot more research’, he says.

Reference:
Todd, W. D., Fenselau, H., Wang, J. L., Zhang, R., Machado, N. L., Venner, A., … & Lowell, B. B. (2018). A hypothalamic circuit for the circadian control of aggression. Nature neuroscience, 1.

http://healthsciences.ku.dk/news/2018/05/researchers-discover-connection-between-circadian-rhythm-and-aggression/

by John Carroll

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The BACE theory in Alzheimer’s R&D is simple. Cut off the flow of amyloid beta to the brain and you can eliminate what is widely believed — though not proven — to be a cause of the disease. Do that, and you could bend the course of this devastating illness in millions of people with mild to moderate forms of the disease.

And Merck $MRK just spent a fortune to demonstrate that it may well be completely wrong.

To be sure, Merck ran a clean study for verubecestat, the leading BACE drug in the clinic, and displayed the data on 1,958 patients for all to see today in the New England Journal of Medicine. Investigators carefully tracked amyloid beta flows in cerebrospinal cords and found that the drug did what it was intended to do, with a dramatic reduction of the toxic protein. 

It had no effect, with patients in the two dosage groups tracking in parallel decline on both cognition and function, the two classic measures for Alzheimer’s. 

The conclusion they reached is that the damage already present in the brains of patients with Alzheimer’s may be too extensive to treat with any BACE drug. And they also concede that the amyloid theory itself may be just flat wrong.

This suggests that once dementia is present, disease progression may be independent of Aβ production or, alternatively, that the amyloid hypothesis of Alzheimer’s disease may not be correct. Because Aβ deposition takes place years before clinical symptoms become apparent, it has been proposed that treatments targeting amyloid should be implemented early in the disease process, before the onset of clinical symptoms.

Soon after this study failed, Merck also threw in the towel on their second pivotal trial, noting it too was a flop. Those data are still being evaluated, but it underscores the belief that all of the BACE studies — including those at Eli Lilly $LLY, partnered with AstraZeneca $AZN, or Biogen $BIIB, allied with Eisai — are headed straight to failure.

Biogen is also rolling the dice on aducanumab, which the company has touted as a leading amyloid beta therapy. But with investigators in the field openly wondering whether the amyloid theory has lured a long lineup into a clinical disaster zone, it’s likely to face growing skepticism that it can develop a safe, effective therapy with just one drug.

This doesn’t by any means eliminate work in the area. True, Pfizer recently pulled out after spending hundreds of millions of dollars on their programs. But startups like Denali believe that new and better technology can give them better odds at success, while Celgene is jumping in with its own new pipeline. Others want to see if combination approaches using tau and amyloid beta together could work. 

Merck’s suggestion about going even earlier in the disease process has also prompted a range of studies in pre-symptomatic patients, while the FDA has signaled its interest in coming up with biomarkers to help speed new studies.

After more than 200 R&D projects ended in disaster, though, Alzheimer’s is looking like an increasingly daunting challenge, with no clear path forward that would inspire confidence among patients with the disease.

https://endpts.com/merck-study-may-signal-doom-for-a-broad-group-of-pivotal-alzheimers-studies/


Psychological sciences doctoral student Marci Horn (left) conducts a name-face memory test as part of a study at the Center for Vital Longevity.

New research from the Center for Vital Longevity (CVL) at The University of Texas at Dallas suggests that subjective complaints about poor memory performance, especially in people over 60, could be a useful early marker for the onset of mild cognitive decline, which sometimes foreshadows Alzheimer’s disease.

Subjective memory is a person’s unscientific self-evaluation of how good his or her memory is, and whether, in that person’s opinion, there has been any worsening of memory through age. While some changes may be undetectable to others and are often too subtle to register on cognitive tests, the person subjectively believes that memory is slipping.

Published recently in Psychology and Aging, the research from Dr. Karen Rodrigue’s lab at CVL examined subjective memory complaints in nearly 200 healthy adults, ages 20 to 94. Previous studies suggest that subjective memory complaints are not necessarily indicative of cognitive decline, and may stem from underlying conditions such as anxiety and depression, which have been shown to impede memory.

The current study measured mood and screened out depressed individuals. Researchers also measured participants for known risk factors for memory loss and Alzheimer’s, such as higher levels of beta-amyloid in the brain and the presence of a gene variant called ApoE4. These factors were taken into account to examine whether subjective memory alone was a reliable correlate of actual memory ability.

The study focused on associative memory — for example, remembering word pairs and name-face pairs. This type of memory is particularly sensitive to age-related decline, and the most common complaint of aging individuals.

The study found that a person’s intuitive or intrinsic assessment of his or her own memory was actually a reliable predictor of performance on the laboratory memory assessment. This result was particularly true for individuals with genetic risk for memory loss.

“Our findings show that subjective memory can be a reliable indicator of memory performance, even in cognitively healthy adults,” said psychological sciences doctoral student Marci Horn, the lead author of the study. “The same people who self-report memory problems may also have other risk factors associated with increased risk of Alzheimer’s disease.”

The researchers also found that men who had higher amyloid levels reported the most subjective memory complaints in the study. Previous studies had not uncovered a sex-specific relationship, nor did they account for the genetic and amyloid risk factors in these associations, the researchers said.

The strongest correlation of subjective memory complaints with actual cognitive performance was in study participants older than 60, when people are generally at greater risk for Alzheimer’s disease.

“It seems that awareness of memory changes may be a reliable indicator of one’s current memory ability, and may serve as another harbinger of future loss, as this relationship was strongest in those with known risk factors for Alzheimer’s disease, namely ApoE4 genotype and beta-amyloid burden in the brain,” said Rodrigue, the senior author of the study and assistant professor in the School of Behavioral and Brain Sciences (BBS). “We are following these individuals over time to further test this idea.”

Dr. Kristen Kennedy, an assistant professor in BBS, also was an author of the study. The research was funded in part by grants from the National Institutes of Health.

https://www.utdallas.edu/news/2018/4/30-32929_Subjective-Memory-May-Play-Role-in-Signaling-Cogni_story-wide.html?WT.mc_id=NewsHomePageCenterColumn